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Introduction. Modern concept corroborates vascular endothelium as a crucial pillar regarding the control of a lot of vascular derived functions in circulatory homeostasis, such as: basal vascular tone and blood pressure, anti-platelet, anti-thrombotic, anti-apoptotic, anti-growing, antiproliferative activity etc. Nitric oxide (NO) and hydrogen sulfide (H 2 S) are considered as important factors in this range of events, because their deficiency is associated with tangible disorders of circulatory homeostasis. Aim of study. Unraveling the role of NO and H2S in circulatory homeostasis regulation and dysfunction. Methods and materials. Was analyzed a material reflected in 20 recent articles found in Google. Results. NO is a gas produced by endotheliocytes from L-arginine under the action of neuroendocrine factors and hemodynamic stress. One of its main functions is vascular dilation due to cGMP formation in the smooth vascular cells. Likewise, NO inhibits expression of proinflammatory cytokines, blunts oxidative stress, decreases platelet adhesion, and mitigates vascular remodeling. H2S is also a gas produced by endotheliocytes from cysteine. It decreases vascular tone due to phosphodiesterase inhibition, upregulates antioxidant enzymes and decreases oxygen radical production, inhibits smooth vascular cell hypertrophy and proliferation, prevents platelet aggregation, has anti-atherogenic effect because decreases the level of homocysteine and LDL-cholesterol. Such serious diseases as arterial hypertension, stroke, and acute myocardial infarction are associated with reduced amounts of NO and H2S. A common pathogenic factor of NO and H2S lack is endothelium injury due to atherosclerosis, systemic inflammation, diabetes. Conclusion. Both NO and H2S, as endothelium derived factors, demonstrate a large palette of beneficial functions concerning the circulatory homeostasis regulation, and their penury due to endothelial damage is viewed as an important trigger and tool of serious cardiovascular maladies, such as arterial hypertension, stroke and acute myocardial infarction. control of a lot of vascular derived functions in circu latory homeostasis, such as: basal vascular tone and blood pressure, anti-platelet, anti-thrombotic, anti-apoptotic, anti-growing, antiproliferative activity etc. Nitric oxide (NO) and hydrogen su lfide (H 2 S) are considered as important factors in this range of events, because their deficiency is associated with tangible disorders of circulatory homeostasis. Aim of study. Unraveling the role of NO and H2S in circulatory homeostasis regulation and dysfunction. Methods and materials. Was analyzed a material reflected in 20 recent articles found in Google. Results. NO is a gas produced by endotheliocytes from L-arginine under the action of neuroendocrine factors and hemodynamic stress. One of its main functions is vascular dilation due to cGMP formation in the smooth vascular cells. Likewi se, NO inhibits expression of proinflammatory cytokines, blunts oxidative stress, decrease s platelet adhesion, and mitigates vascular remodeling. H2S is also a gas produced by endotheliocyt es from cysteine. It decreases vascular tone due to phosphodiesterase inhibition, upregulates antioxidant enzymes and decreases oxygen radical production, inhibits smooth vascular cell hyper trophy and proliferation, prevents platelet aggregation, has anti-atherogenic effect because decreases the level of homocysteine and LDL-cholesterol. Such serious diseases as arterial hyper tension, stroke, and acute myocardial infarction are associated with reduced amounts of NO and H2S. A common pathogenic factor of NO and H2S lack is endothelium injury due to atherosclerosis, s ystemic inflammation, diabetes. Conclusion. Both NO and H2S, as endothelium derived factors, demonstrat e a large palette of beneficial functions concerning the circulatory homeost asis regulation, and their penury due to endothelial damage is viewed as an important trigger and tool o f serious cardiovascular maladies, such as arterial hypertension, stroke and acute myocardial infarction. |
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